Obesity continues to grow around the globe, an

epidemic

is known to affect millions. The issue more widespread and common that thought to be. In fact, many of us might know or be related to individuals that struggle with the effects of obesity. Because the problem is so widespread and common, several misconceptions of obesity still exist today, and many scientific communities are still divided upon several of its issues. There seems to be no progression in the matter, it seems to have come to a full stop without deriving any definitive conclusions and answers. The problem concerning obesity, so diverse in its form leads to so many questions concerning it to exist. Because of so many questions and the lack of substantial answers, lines concerning obesity are extremely blurred, there is no definitive side which is black and white, or, right and left.

One of the most prevalent questions concerning obesity is around is its genetic and environmental factors. Still, medical communities question and divide themselves upon whether obesity is genetic in nature. Solid evidence, of gene expression and regulation of certain proteins, hormones, and or polypeptides, such as adispin, leptin, pro-opiomelanocortin, and melanocortin, directly affect one’s obesity risk based on some genetic predispositions.  However, criticism on the genetics of obesity shines light on many environmental factors, such as eating habits, exercise habits, socioeconomic status, drug use, and so one forth.

Recent research indicates certain hereditary traits regulate gene expression functions, resulting in one’s development of obesity. One study finds that adispin gene expression precedes metabolic malfunction, resulting in binge-feeding and abnormal weight gain1. The research observes messenger RNA expression and regulation in several adipocyte genes in rats with metabolic syndromes and obese phenotypes.1 The two rat types used, each with homozygous-recessive birth related obesity conditions for specific alleles at chromosomal loci 4 and 6.1 Results indicated that controlled diets had no significant increase in adispin messenger RNA levels; where proper concentrations regulate energy mobility and fitness related functions1. However, the opposing side conducts a cross-sectional study concerning the relationship between obesity and breastfeeding in young children.2 511 male and female students, aged 7 were subjected at random, where their weights and heights were measured, along with their mothers’.2 The study measured both breast and formula fed children, along with the time they were introduced to solid diets.2 Through data, it was found that children introduced to solid foods earlier on developed and were at risk for a higher body mass index, due to a higher energy intake, causing room for concern as breastfeeding showed no contribution in body mass index.2

Both these experiments, regardless of their side of debate present strong data validated with proper experimental design. The supporting study, in great detail explained all findings, and how they supported and related to their hypothesis, and their control and experimental groups were clearly labelled, and all information concerning them was explained thoroughly. In addition, the visual proof indicated in the experiment, such that of their western blotting diagrams measuring adispin mRNA1, for their experimental and control groups. In addition, several visual aids, such as graphs, tables, and charts were presented which aided the validity of their research. On the other hand, however, the nurture side of the debate seems to be lacking in some respects due to certain limitations. The experiment was confounded by several unknown environmental variables that were difficult controlled for.2 Another limitation the experiment mentioned was that birth order and weight was measured based on the mother’s estimate, which may have led to inaccuracies in the data.2 Lastly, the data presented in the study did not differentiate between ‘lean’ and ‘fat’ mass when measuring body mass indexto measure obesity levels in the children.2

Research studying the effects of leptin resistance in obese mutant mice find that abnormal increases in body mass index is due to leptin receptor signalling and rejection defects, originating from certain genetic mutations concerned with primary cilia.3 The experiment argues that ciliac malfunction and loss affects neurons in the hypothalamus that is responsible for controlling eating behaviour.3 Demographics in Spain measuring genetic variation in the leptin gene promoter’s risk concerning obesity through a case-controlled study on 909 participants, found that Leptin resistance among the gene pool was homozygous recessive and was less common that the controlled, healthy population that were majorly homozygous dominant.4 which in their own ways significantly increased and decreased an individual’s obesity risk4. However, the same study shows, that individuals with the homozygous healthy dominant gene for leptin, whom had unhealthy lifestyles and lower quality of living were more prone to obesity as well4, thus bringing in an environmental factor into the argument.

The first study experimenting upon leptin resistance in mice tests several genes present in adipose cells, in genetically mutant mice.3 When testing and studying several genes, the validity of the data is increased. The experiment had little to no flaws, as all aspects of the experiment, such as background information, additional, methods, control and experimental groups, results, discussions, and additional finds were thoroughly explained. The research had plentiful of visual aids to back up their claims, such as through graphs, charts, and tables; overall, scientifically the experiment was compelling and well done. There was little and weak proof backing up the opposition side Some evidence was available through the second study mentioned above, as it directly contradicted itself, proving that other environmental and confounding factors have an effect on obesity and leptin resistance. Since there were many confounded variables to control for, such as drug addiction, gender, and socioeconomic status, the experiment struggled upon accurately measuring genetic influence on obesity in regard to inherited leptin resistance.

Another major genetic risk factor upon obesity is the expression of melanocortin, a series of peptide hormones regulated by the POMC (pro-opiomelanocortin) polypeptide. Several studies experimenting on lab rats, such that in the journal of

PNAS,

studied mice lacking POMC due to inactivating gene mutations resulted in feeding and over-feeding of higher fat diets.5 In the experiment, mice with compromised POMC function, severely increased BMI, or in other words, obesity severity, risks, and rates.5 Other similar studies on mice, find the effect of POMC gene expression on melanocortin regulation directly link with fat and sucrose preference signalling in humans6, whereas in mice, the gene expression and regulation of POMC and melanocortin to some extent, controlled the perceived degree of appetizing food appeal.7 In mice, the receptors of Melanocortin have shown to reduce the appeal of unhealthy or appetizing foods, and supress hunger.7 When these melanocortin receptors are faulty, and are deficient, severe obesity, developed early in life, being melanocortin obesity syndrome, as a result.7 However, evidence opposing this research highlight the importance of the effects of glucose sugar on leptin found on POMC neurons in the brain’s hypothalumus.8 The research indicates that the hunger-supressing characteristics of leptin are highly compromised with continued and increased intake of glucose in one’s diet.8 The POMC’s electrical properties in the brain’s hypothalamus directly, thus correlate with glucose concentrations, as indicated in the results of the experiment.8

Although the study of glucose levels and POMC holds a significant claim backed with solid evidence, the nurture side of the debate is severely supressed by the quantity of the supporting, genetic based evidence. Far more studies have been conducted concerning genetic effects on POMC and melanocortin, than the environmental based factors. Furthermore, the presented genetic based evidence includes all the necessary elements of an experiment, that can easily be replicated with minimal ethical barriers. The materials, methods, results, and discussions were thoroughly explained, with the indication of all appropriate controls and experimental groups, such as the environment and dietary habits, of the lab mice. In addition, the experiments explained in support of ‘genetic obesity’ used statistical analysis, visual aid, and performed several trails and repetitions of their experiments which increased their validity. In detail, they discussed ways in which mice were testing upon, their care and handling protocols, along with acknowledging other miscellaneous measures positively highlighting ethical protocols practiced when experimenting upon lab mice. In addition, at least one experiment applied directly to humans as it was tested on humans, with ethical conditions in mind, which increases research and data relevance, thus providing stronger argumentation. The opposing evidence, however, did not have well established and clear enough control groups established in their research, which further questions the quality of the experiment. In addition, living mice were not used, but coronal brain slices of transgenic mice only two-four weeks of age.8 This not only creates certain ethical concerns for the animals, but the validity of the results as results may have varied between live, brain intact mice, from pre-maturely killed, dissected, transgenic mice.8

Although both sides have evidence backing up their sides of the argument, the opposing side, that obesity is due to environmental concerns is lacking in several aspects when compared to the supportive, genetic side of the debate. The pro-genetic experiments and studies conducted were much more systematic in nature and controlled for their variables better. The experiments, scientifically were thorough when compared to the environmental side, and were less confounded. This increased the reliability and variability of their results, and thus, held far more convincing, and solid results, along with their statistical analysis. Thus, to argue, sufficient, well-based evidence exists that obesity and obesity developmental risk is predisposition and is heavily influenced and associated with genetic factors.


References in Nature Style:

  1. Flier, J. et al. Severely Impaired Adispin Expression in Genetic and Acquired Obesity.

    Science

    237, 405-408, 1987
  2. Vafa, M. et al. Relationship between Breastfeeding and Obesity in Childhood.

    Journal of Health, Population and Nutrition

    30, 303-310, 2012
  3. Berbari, N.F. et al. Leptin resistance is a secondary consequence of the obesity in ciliopathy mutant mice.

    Proceedings of the National Academy of Sciences of the United States of America

    19, 7796-7801, 2013
  4. Portolés, O. et al. Effect of Genetic Variation in the Leptin Gene Promoter and the Leptin Receptor Gene on Obesity Risk in a Population-Based Case-Control Study in Spain.

    European Journal of Epidemiology

    21, 605-612, 2006
  5. Challis, B.G. et al. Mice Lacking Pro-Opiomelanocortin Are Sensitive to High-Fat Feeding but Respond Normally to the Acute Anorectic Effects of Peptide- YY3-36.

    Proceedings of the National Academy of Sciences of the United States of America

    101, 4695-4700, 2004
  6. Van der Klaauw, A.A. et al. Divergent effects of central melanocortin signalling on fat and sucrose preference in humans.

    nature communications

    7, 13055, 2016
  7. L,B. et al. Melanocortin-4 receptor mutations paradoxically reduce preference for palatable foods.

    Proceedings of the National Academy of Sciences of the United States of America

    110, 7050-7055, 2013
  8. Ma, X. Zubcevic, L. Ashcroft, F.M.

    Proceedings of the National Academy of Sciences of the United States of America

    28, 9811-9816, 2008

Rational:

Obesity is one of the fastest spreading health concerns around the globe, and even if this may not impact us directly, it can take a great personal affect. In America alone, over two thirds of the country’s population suffer from body mass indexes higher than the normal, or ideal. In relation to the statistics, many of us may know a loved one or friend suffering from the medical, and physiological, and or psychological effects of obesity. Many individuals, from my own personal experience, have been heavily stigmatized on their excess weight, and are distanced as equal members of society. The high emphasis put upon beauty, having an ideal body shape, and so on forth adds further unnecessary pressures and stresses on one’s life. However, it’s important to realize that many cases exist where substantial exercise, healthy dietary habits, and reduced stress does not work for everyone, especially those prone to certain genetic predispositions, resulting with heavier phenotypes. Rather than seeing the obese the result of a failed society because of a technology dependant world and the presence of an uncontrollable fast food culture, awareness is needed upon other possibilities and factors leading to obesity. Furthermore, continued research and awareness upon obesity and opens pathways for new medical miracles, and treatment options for individuals at greater risk or are already directly impacted by this health concern. The further advancement of technology, and knowledge in the scientific community, gives rise to certain genetic fields, such that of epigenetics, and cloning, which may aid and or even diminish the genetic, predisposed effects on obesity, and obesity risk.


 

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